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Placental Hypoxia-Induced Ferroptosis Drives Vascular Damage in Preeclampsia.
Circ Res
January 2025
Lunenfeld-Tanenbaum Research Institute, Sinai Health System, Toronto, Ontario, Canada (C.P., S.A., J.W.A., R.L., F.N., J.S., I.C.).
Background: Iron is an essential micronutrient for cell survival and growth; however, excess of this metal drives ferroptosis. Although maternal iron imbalance and placental hypoxia are independent contributors to the pathogenesis of preeclampsia, a hypertensive disorder of pregnancy, the mechanisms by which their interaction impinge on maternal and placental health remain elusive.
Methods: We used placentae from normotensive and preeclampsia pregnancy cohorts, human H9 embryonic stem cells differentiated into cytotrophoblast-like cells, and placenta-specific preeclamptic mice.
Endothelium Modulates the Prothrombotic Phenotype of Factor V Leiden: Evidence From an Ex Vivo Model.
Arterioscler Thromb Vasc Biol
January 2025
Institute of Experimental Hematology and Transfusion Medicine, University Hospital Bonn, Germany.
Background: Clinical expressivity of the thrombophilic factor V Leiden (FVL) mutation is highly variable. Recently, we demonstrated an increased APC (activated protein C) response in asymptomatic FVL carriers compared with FVL carriers with a history of venous thromboembolism (VTE) after in vivo coagulation activation. Here, we further explored this association using a recently developed ex vivo model based on patient-specific endothelial colony-forming cells (ECFCs).
View Article and Find Full Text PDFVascular HIF2 Signaling Prevents Cardiomegaly, Alveolar Congestion, and Capillary Remodeling During Chronic Hypoxia.
Arterioscler Thromb Vasc Biol
January 2025
Metabolic and Immune Diseases Department, Biomedical Research Institute Sols-Morreale (IIBM), National Research Council (CSIC), Autonoma University of Madrid, Spain (T.A.-G., S.M.-T., R.C.-M., S.U.-B., S.M.-P.).
Background: Hypoxia is associated with the onset of cardiovascular diseases including cardiac hypertrophy and pulmonary hypertension. HIF2 (hypoxia-inducible factor 2) signaling in the endothelium mediates pulmonary arterial remodeling and subsequent elevation of the right ventricular systolic pressure during chronic hypoxia. Thus, novel therapeutic opportunities for pulmonary hypertension based on specific HIF2 inhibitors have been proposed.
View Article and Find Full Text PDFLong-term results of lymphedema treatment with Combined lymph node transfer and collagen scaffolds: An Observational Study.
JPRAS Open
March 2025
Department of Plastic Surgery, Aristotle University of Thessaloniki, School of Medicine, Papageorgiou General Hospital, Thessaloniki, 54603, Greece.
Aim: Vascularized lymph node transfer (VLNT) accelerates growth factor secretion, lymphatic endothelial cell migration toward the interstitial flow and lymphagiogenesis in a multidirectional pattern. Our observational study aimed to examine the hypothesis that nanofibrillar collagen scaffolds (NCS) combined with VLNT can provide guided lymphagiogenesis creating long-lasting lymphatic pathways.
Methods: Twenty-four patients (21 female, 3 male) underwent a lymphatic microsurgery for upper ( = 11) or lower ( = 13) limb secondary lymphedema and completed at least 18 months follow-up were selected and equally divided in 2 groups; Group-A underwent VLNT, Group-B underwent combined VLNT and NCS procedure.
Unphysiological lung strain promotes ventilation-induced lung injury via activation of the PECAM-1/Src/STAT3 signaling pathway.
Front Pharmacol
January 2025
Department of Emergency Intensive Care Unit, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Introduction: In patients with acute respiratory distress syndrome, mechanical ventilation often leads to ventilation-induced lung injury (VILI), which is attributed to unphysiological lung strain (UPLS) in respiratory dynamics. Platelet endothelial cell adhesion molecule-1 (PECAM-1), a transmembrane receptor, senses mechanical signals. The Src/STAT3 pathway plays a crucial role in the mechanotransduction network, concurrently triggering pyroptosis related inflammatory responses.
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